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I’m not a conspiracy theorist. Really. But as I wade through the thicket of science studies and rhetoric of science readings I have on my desk, I am more and more impressed with the power of paradigmatic thinking to distort how scientific knowledge is produced and disseminated.

Daisy Zamora and company have once again climbed in their wayback machine to reanalyze data from the Minnesota Coronary Survey, which began in 1968. The vegetable oil intervention reduced saturated fat intake by about half and cholesterol consumption by about two-thirds, while nearly tripling the intake of polyunsaturated fat. Surprise, surprise–they found that although the vegetable oil intervention reduced cholesterol levels, the intervention also led to more heart attacks and increased risk of death. [The press release on the study is here; the study itself is here.]

Let me just add that the original study outcomes–which did not support the diet-heart hypothesis even then–were not published until many years after the study ended, in fact, after its primary investigator retired.

Zamora and her co-investigators politely refer to these sort of anomalies as “incomplete publication,” as in:

“… incomplete publication of important data has
contributed to the overestimation of benefits – and the underestimation of potential risks – of replacing
saturated fat with vegetable oils rich in linoleic acid.”

All I want to say, before going back and burying my head once again in my books, is that

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I know, I know. I never post. I never call. I don’t bring you flowers. It’s a wonder we’re still together. I have the usual list of excuses:

1) GRADUATE SCHOOL

But before I disappear off the face of the interwebz once again, I thought I share with you a quickie post on the science behind our current Dietary Guidelines. Even as we speak, the USDA and DHHS are busy working on the creation of the new 2015 Dietary Guidelines for Americans, which are shaping up to be the radically conservative documents we count on them to be.

For just this purpose, the USDA has set up a very large and impressive database called the Nutrition Evidence Libbary (NEL), where it conducts “systematic reviews to inform Federal nutrition policy and programs.” NEL staff collaborate with stakeholders and leading scientists using state-of-the-art methodology to objectively review, evaluate, and synthesize research to answer important diet-related questions in a manner that allows them to reach a conclusion that they’ve previously determined is the one they want.

In the NEL, they break the evidence up into “cardiovascular” and “diabetes” so I’ll do the same, which means we are really asking: What is the effect of saturated fat (SFA) intake on increased risk of cardiovascular disease?

Spoiler alert–here’s the answer: “Strong evidence” indicates that we should reduce our intake of saturated fat (from whole foods like eggs, meat, whole milk, and butter) in order to reduce risk of heart disease. As Gomer Pyle would say, “SUR-PRIZE, SUR-PRIZE.”

Aaaaaaaand . . . here’s the evidence:

The 8 studies rated “positive quality” are in blue; the 4 “neutral quality” studies are in gray. The NEL ranks the studies as positive and neutral (less than positive?), but treats them all the same in the review. Fine. Whateverz.

According to the exclusion criteria for this question, any study with a dropout rate of more than 20% should be eliminated from the review. These 4 studies have dropout rates of more than 20%. They should have been excluded. They weren’t, so we’ll exclude them now.

Also, according to NEL exclusion criteria for this question, any studies that substituted fat with carbohydrate or protein, instead of comparing types of fat, should be excluded. Furtado et al 2008 does not address the question of varying levels of saturated fat in the diet. In fact, saturated fat levels were held constant–at 6% of calories–for each experimental diet group. So, let’s just exclude this study too.

One study–Azadbakht et al 2007–was conducted on teenage subjects with hypercholesterolemia. Since the U.S. Dietary Guidelines are not meant to treat medical conditions and are meant for the entire population, this study should not have been included in the analysis. Furthermore, the dietary intervention not only lowered saturated fat content of the diet but cholesterol content too. So it would be difficult to attribute any outcomes only to changes in saturated fat intake. The study should not have been included, so let’s take care of that for those NEL folks.

In one study–Buonacorso et al 2007–total cholesterol levels did not change when dietary saturated fat was increased: “Plasma TC [total cholesterol] and triacylglycerol levels were NS [not significantly] changed by the diets, by time (basal vs. final test), or period (fasting vs. post-prandial) according to repeated-measures analysis.” This directly contradicts the conclusion of the NEL. Hmmmm. So let’s toss this study and see what’s left.

In these four studies, higher levels of saturated fat in the diet made some heart disease risk factors get worse, but other risk factors got better. So the overall effect on heart disease risk was mixed or neutral. As a result, these studies do not support the NEL conclusion that saturated fat should be reduced in order to reduce risk of heart disease.

That leaves one lone study. A meta-analysis of eleven observational studies. Seeing as the whole point of a meta-analysis is to combine studies with weak effects to see if you end up with a strong one, if saturated fat was really strongly associated with heart disease, we should see that, right? Right. What this meta-analysis found was that among women over 60, there is no association between saturated fat and coronary events or deaths. Among adult men of any age, there is no association between saturated fat and coronary events or deaths. Only in women under the age of 60 is there is a small inverse association between risk of coronary events or deaths and the reduction of saturated fat in the diet. That sounds like it might be bad news—at least for women under 60—but this study also found a positive association between monounsaturated fats—you know, the “good fat,” like you would find in olive oil—and risk of heart disease. If you take the results of this study at face value–which I wouldn’t recommend–then olive oil is as bad for you as butter.

So there’s your “strong” evidence for the conclusion that saturated fat increases risk of heart disease.

Just recently, Frank Hu of the 2015 Dietary Guidelines Advisory Committee was asked what we should make of the recent media attention to the idea that saturated fat is not bad for you after all (see this video at 1:06:00). Dr. Hu reassured us that, no, saturated fat still kills. He went on to say that the evidence to prove this, provided primarily by a meta-analysis created by USDA staffers (and we all know how science-y they can be), is MUCH stronger than that used by the 2010 Committee.

Well, all I can say is: it must be. Because it certainly couldn’t be any weaker.

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Move over saturated fat and cholesterol. There’s a new kid on the heart disease block: TMAO.

TMAO is not, as I first suspected, a new internet acronym that I was going to have to get my kids to decipher for me, while they snickered under their collective breaths. Rather, TMAO stands for Trimethylamine N-oxide, and it is set to become the reigning king of the “why meat is bad for you” argument. Former contenders, cholesterol and saturated fat, have apparently lost their mojo. After years of dominating the heart disease-diet debate, it turns out they were mere poseurs, only pretending to cause heart disease, the whole time distracting us from the true evils of TMAO.

The news is, the cholesterol and saturated fat in red meat can no longer be held responsible for clogging up your arteries. TMAO, which is produced by gut bacteria that digest the carnitine found in meat, is going to gum them up instead. This may be difficult to believe, especially in light of the fact that, while red meat intake has declined precipitously in the past 40 years, prevalence of heart disease has continued to climb. However, this is easily accounted for by the increase in consumption of Red Bull—which also contains carnitine—even though it is not, as some may suspect, made from real bulls (thank you, BW).

Here to explain once again why we should all be afraid of eating a food our ancestors ignorantly consumed in scandalous quantities (see what happened to them? they are mostly dead!) is the Medical Media Circus! Ringleader for today is the New York Times’ Gina Kolata, who never met a half-baked nutrition theory she didn’t like (apparently Gary Taubes’ theory regarding carbohydrates was not half-baked enough for her).

Step right up folks and meet TMAO, the star of “a surprising new explanation of why red meat may contribute to heart disease” (because, frankly, the old explanations aren’t looking too good these days).

We know that red meat maybe almost probably for sure contributes to heart disease, because that wild bunch at Harvard just keeps cranking out studies like this one, Eat Red Meat and You Will Die Soon.

This study and others just like it definitely prove that if you are a white, well-educated, middle/upper-middle class health professional born between 1920 and 1946 and you smoke and drink, but you don’t exercise, watch your weight, or take a multivitamin, then eating red meat will maybe almost probably for sure increase your risk of heart disease. With evidence like that, who needs evidence?

Flying like the Wallenda family in the face of decades of concrete and well-proven assumptions that the reason we should avoid red meat is because of its saturated fat and cholesterol content, the daring young scientists who discovered the relationship between TMAO and heart disease “suspected that saturated fat and cholesterol made only a minor contribution to the increased amount of heart disease seen in red-meat eaters” [meaning that is, the red-meat eaters that are white, well-educated, middle/upper-middle class health professionals, who smoke and drink and don’t exercise, watch their weight, or take a multivitamin; emphasis mine].

Perhaps their suspicions were alerted by studies such as this one, that found that, in randomized, controlled trials, with over 65 thousand participants, people who reduced or changed their dietary fat intake didn’t actually live any longer than the people who just kept eating and enjoying the same artery-clogging, saturated fat- and cholesterol-laden foods that they always had. (However, this research was able to determine that a steady diet of broiled chicken breasts does in fact make the years crawl by more slowly.)

Exactly how TMAO increases the risk of heart disease, nobody knows. But, good scientists that they are, the scientists have a theory. (Just to clarify, in some situations the word theory means: a coherent group of tested general propositions, commonly regarded as correct. This is not one of those situations.) The researcher’s think that TMAO enables cholesterol to “get into” artery walls and prevents the body from excreting “excess” cholesterol. At least that’s how it works in mice. Although mice don’t normally eat red meat, it should be noted that mice are exactly like people except they don’t have Twitter accounts. We know this because earlier mouse studies allowed scientists to prove beyond the shadow of a doubt that dietary cholesterol and saturated fat cause heart disease mice definitely do not have Twitter accounts.

Look, just because the scientists can’t explain how TMAO does all the bad stuff it does, doesn’t mean it’s not in there doing, you know, bad stuff. Remember, we are talking about molecules that are VERY VERY small and really small things can be hard to find–unless of course you are on a scientific fishing expedition.

What will happen to the American Heart Association’s seal of approval now that saturated fat and cholesterol are no longer to be feared?

Frankly, I’m relieved that we FINALLY know exactly what has been causing all this heart disease. Okay, so it’s not the saturated fat and cholesterol that we’ve been avoiding for 35 years. Heck, everybody makes mistakes. Even though Frank Sacks and Robert Eckel, two scientists from the American Heart Association, told us for decades that eating saturated fat and cholesterol was just greasing the rails on the fast track to death-by-clogged-arteries, they have no reason to doubt this new theory. And even though they apparently had no reason to doubt the now-doubtful old theory, at least not until just now—as a nation, we can rest assured that THIS time, they got it right.

Now that saturated fat and cholesterol are no longer Public Enemies Number One and Two, whole milk, cheese, eggs, and butter—which do not contain red meat—MUST BE OKAY! I guess there’s no more need for the AHA’s dietary limits on saturated fat, or for the USDA Guidelines restrictions on cholesterol intake, or for those new Front of Package labels identifying foods with too much saturated fat. Schools can start serving whole milk again, butter will once again be legal in California, and fat-free cheese can go back to being the substance that mouse pads are made out of. Halla-freaking- looyah! A new day has dawned.

But—amidst the rejoicing–don’t forget: Whether we blame saturated fat or cholesterol or TMAO, meat is exactly as bad for you now as it was 50 years ago.

The best that we can say is that since the 1970s, rates of myocardial infarction have decreased slightly—but only in white folks.

If the current health prescription is valid, then we should see dramatic differences in rates of disease and mortality between those who follow the prescription and those who don’t, and we should see clear and strong associations between “healthy” food choices and good health (because the same people eating a “healthy” diet are also taking care of their health in other ways). Yet this is not what we see.

Is it possible that our low-fat diet has removed some protective factors from our nutritional profile and exposed us to increased levels of nutrients that have negative impacts on health? I think it is, and a recent study in BMJ supports this notion.

I am a long-time admirer of one of the researchers, Daisy Zamora, and she is a good friend of mine. She’d been dropping hints about this great study she was working on for a while now—but was sworn to secrecy and now I know why. What she and her co-investigators have uncovered is data from a long-ago diet study, conducted from 1966-1973. It’s a decently large, well-run, randomized controlled trial that replaces saturated fat with safflower oil, a vegetable oil particularly high in one kind of PUFA—omega-6 (n-6) linoleic acid—and low in another kind of PUFA—omega-3 (n-3) alpha linolenic acid. The idea was that replacing “bad” saturated fat with “healthy” vegetable oil in men with premature coronary heart disease would improve survival. This did not turn out to be the case. For some reason, though, the original study only reported all-cause mortality and not deaths from cardiovascular disease and coronary heart disease.

Daisy and her co-investigators climbed into their way-back machine and this is what they found: Not only did the participants in the intervention group have an increased risk of all-cause mortality, but they had an increased risk of death from cardiovascular disease and coronary heart disease.

The blue line is the safflower oil group; the red line is the control group. To put it rather simplistically, the widening gap between the two groups means the intervention group died a lot faster than the controls.

Although the switch to safflower oil did lower total cholesterol, these reductions didn’t help those participants live any longer than those who kept eating saturated fat. In fact, as the authors note, “the increased risk of death in the intervention group presented fairly rapidly and persisted throughout the trial.” (Hmm. Maybe this whole “cholesterol lowering” thing isn’t as important as we thought.)

Furthermore, the authors go on to point out that the relationship between linoleic acid consumption and increased mortality was particularly robust in smokers and drinkers, “suggesting that diets high in n-6 [linoleic acid] may be particularly detrimental in the context of oxidative stress induced by smoking and alcohol.”

Everyone knows that if you are a smoker you should quit and that alcohol should be used in moderation. But, with this evidence in mind, if you decided to keep on smoking and/or you want to drink immoderately, you may want to consider a breakfast of eggs and bacon rather than whole wheat toast and “heart healthy” margarine before you do.

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I was a young adult in the 1980s, just after the first Dietary Guidelines rocked our world. Yes, I remember the bacon-and-eggs frowny face on the cover of Times. It was in the checkout lane as I was buying my low-fat, fruit-and-sugar filled yogurt. Of course, I would soon come to my senses and switch to fat-FREE yogurt. Why? Because animal fat, including whatever remaining milkfat was in my yogurt, has Very Scary saturated fat in it. Did I know what that meant? Of course not. But I do now.

At my house, we like to joke that fats suffer from a serious PR problem (that’s what passes for humor around here). It’s so easy to think FAT=FAT. And “saturated” fat sounds even more ominous and creepy, saturating our blood with icky gooey . . . um . . . somethingy. Surely those loverly ladies Mona Unsaturated Fatty Acid (MUFA) and Polly Unsaturated Fatty Acid (PUFA)—Moofa and Poofa to friends—are better company to keep. That seems to be what the folks at Harvard think, anyway.

Enter actual biochemistry.

In biochem class, I found out that “saturated” simply meant that the carbon chain of a fatty acid was fully “saturated” with hydrogen and therefore, there are no double bonds. That’s not very scary.

Yeah, but my BFF, Polly Unsaturated, as it turns out, was more of a frenemy than I thought.

Just about everyone has heard of antioxidants. They are why we are supposed to eat fruitsandvegetables. The point of antioxidants is to deal with “free radicals,” which sound like some kind of hippie flashback, but is simply a term to describe a molecule with one or more unpaired electrons that reacts easily with other molecules. In cell membranes, they can really cause problems because the long, straight profile of a fatty acid chain can get oxidized by reacting with a free radical, causing it to bend, which weakens the integrity and functionality of the membrane.

Even a middle-schooler can see (I know, I asked one) that this just doesn’t look good for the cell membrane. It gets worse. The reaction that occurs not only damages that particular fatty acid, but is a self-propagating reaction. It starts and then it doesn’t stop—until an antioxidant comes along. The results: lotsa crooked Poofas.

The academic-industrial complex has recited to us the story that we should increase the consumption of corn and soybean oils—which contain about 60% of these fatty acids—because they are so good for us. They have the population studies to prove it. But this tale is as twisted as an oxidized Poofa. Ever since 1980, when we told people to start eating more Poofas, folks who are concerned about their health have eaten more Poofas. While we don’t really know if consuming corn and soybean oil will make you a healthier person, we do know that caring about your health will. And even though people who care about their health are generally more healthy than people who aren’t, as a population we are all less healthy. Could it be the Poofas that have saturated our food supply?

By sheer coinkydink, corn and soybean oils happen to be big moneymakers for food processors. That’s why I really get bent out of shape when we’re told that we grow soy and corn so we can feed it to cows. That’s like saying we drill for oil so we can make lipstick.

We may find out in the long run that it isn’t just our increase in carbohydrates, but our increase in Poofa–and the corresponding decrease in not-so-scary saturated fat–that is truly at the root of our current health crises. In which case, miss Poofa can kiss my butter.

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One of the enduring myths of our current nutrition culture is that Americans don’t follow recommendations–have never followed them–because if we had, this obesity thing wouldn’t have happened. According to the 2010 Dietary Guidelines Advisory Committee Report, “average American food patterns currently bear little resemblance to the diet recommended in the 2005 Dietary Guidelines for Americans.”

As proof, the following figure is provided:

FIGURE 1: Americans don’t follow dietary recommendations!

It seems pretty obvious that Americans are woefully off-base when it comes to eating anything close to what the USDA and HHS have been recommending for the past thirty years. I would bet my RD certification that this figure will be shown in PowerPoints across the land to demonstrate—to the accompaniment of much hand-wringing—how we must “make the healthy choice the easy choice” for those poor, dumb Americans who will otherwise just eat themselves into obesity and ruin airplane trips for the rest of us.

Aside from the fact that Americans are being evaluated on whether or not they follow the Guidelines, rather than whether or not the Guidelines are actually appropriate, there are some serious “truth in advertising” issues going on with this figure.

First, note the data collection time points: National Health and Nutrition Examination Surveys from 2001-2004, and 2005-2006. And the fun begins . . .

1) The figure shows that we eat too many calories from SoFAS. But this concept was not part of the Guidelines until the 2010 Dietary Report, the report that contains this figure. In other words, Americans are being held to standards that hadn’t even been created yet.

2) The saturated fat “cut-off” is based on a 7% of calories. The recommended limit for saturated fat at the time the data were collected and at the time this document was written is 10% of calories, not 7%.

3) The standards for whole grain consumption given in the Guidelines that the public would be familiar with when the data were collected were pretty vague: “Choose a variety of grains daily, especially whole grains” (from the 2000 Dietary Guidelines). I don’t know how this translates into an absolute amount of whole grains that Americans don’t consume.

4) The report that contains this figure (the 2010 Dietary Guidelines Advisory Committee Report) indicates that added sugars should be less than 25% of calories. Current research indicates that added sugar consumption by Americans is around 16% of total calories (Welsh et al, 2010, JAMA). According to this figure, Americans consume 242% more added sugars than recommended. Another mystery.

5) In the fine print, it says that the sodium cut-off is based on the recommended Adequate Intake (AI) amount. The AI amount is a “goal for adequate intake,” and, as such, is more of a floor than a ceiling. The AI amount is currently set at 1500 mg of sodium for adults. On the other hand, the Dietary Guidelines that were in effect at the time the data were collected set sodium recommendations at 2400 mg (2000 DGs) and 2300 mg (2005 DGs) per day.

Americans don’t follow the Guidelines–but the standards being used in a number of cases aren’t even part of the Guidelines?

Here’s a different perspective on whether or not Americans are following dietary recommendations:

Since 1980, Americans have been told to increase their carbohydrate consumption and reduce their fat intake. Since 1980, we’ve done just that. American’s consumption patterns fall within the recommended AMDR levels, with the exception of saturated fat, which—at 11% of total calories—is just slightly more than the recommended limit of 10% of calories. (If you are interested in just exactly how well Americans have complied with the dietary recommendations of the past 30 years, you can find the gory details here.) Far from being careless and casual consumers of anything and everything, Americans have radically shifted their eating patterns to match recommendations.

So why don’t Americans get any credit for actually lowering their fat intake and raising their carbohydrate intake, as we were told to do? I think there are a couple of things behind that.

First, I think one of the purposes of information like that presented in Figure 1 is to make sure the responsibility for overweight and obesity continues to rest squarely on the chubby little shoulders of Americans themselves and in no way reflects a possible lack of appropriateness of (or—gasp!—good scientific basis for) the Guidelines themselves. This is an attitude that pervades the Dietary Guidelines.

This is where recommendations become fanaticism. According to Neil Postman, “the key to all fanatical beliefs is that they are self-confirming.” The USDA and HHS seem unwilling to even acknowledge that the dietary shift that has occurred during the past thirty years has actually been in the direction of compliance with recommendations; in fact–according to Figure 1–they are willing to fudge the numbers to prove otherwise. That’s not nice, and it’s sure not science.